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. 2011 Jun 13;118(5):1350–1358. doi: 10.1182/blood-2011-03-345272

Figure 3.

Figure 3

A 2-gene model is independently prognostic of survival in DLBCL and a composite model integrating IPI. (A) Performance of the TGS comprising expression of LMO2 and TNFRSF9 as evaluated in the training (DLBCL1) cohort. Tertiles of the TGS define 3 risk groups with distinct Kaplan-Meier estimates of survival (high risk, TGS > −0.91; intermediate risk, −0.91 ≥ TGS > −1.60; and low risk, TGS ≤ −1.60). TGS retains prognostic power within GCB (B) and ABC (C) subtypes of DLBCL treated with R-CHOP. Cases “unclassified” for cell of origin were excluded. (D) Kaplan-Meier estimates of strata using tertiles of a composite risk score integrating TGS and IPI (TGS-IPI). Depicted P values reflect log-likelihood estimates. (E) Distribution of the TGS-IPI and its relationship to survival in the training cohort, with survival modeled as a continuous function of the composite score. Tertiles of the TGS-IPI define strata are depicted in panel D, where means and 95% CI reflect Kaplan-Meier estimates at 2 years. Scores for individual patients are depicted as a “rug” above the x-axis. By applying thresholds derived from tertiles in the R-CHOP–treated training cohort (supplemental Figure 5), the TGS also stratifies OS of patients in 2 test cohorts treated with CHOP (DLBCL2, panel F, P < .0001, HR = 1.8 [1.4-2.3]; and DLBCL3, panel G, P = .0002, HR = 2.0 [1.4-2.9]).